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A Cases

Publications and source records attributed to A Cases.

At least 19 recordsLinked to original sources

Reticulated platelets in uremic patients: effect of hemodialysis and continuous ambulatory peritoneal dialysis.

Platelet RNA content can be detected by flow cytometry using thiazole orange staining to identify platelets recently released into the circulation. We studied platelet RNA content and platelet function in uremic patients under different treatment regimens. Four groups were studied: (I) 15 end-stage renal disease (ESRD) patients (10M/5F) on maintenance hemodialysis (HD); (II) 11 ESRD patients (6M/5F) on continuous ambulatory peritoneal dialysis (CAPD); (III) 8 patients with chronic renal failure managed conservatively (5M/3F); and (IV) 34 controls (20M/14F). A double color labeling technique using a phycoerythrin-tagged antibody against glycoprotein Ib (CD42b) and RNA labeling by thiazole orange was performed and read by flow cytometry. Aggregation studies were made in platelet-rich plasma using ADP, epinephrine, collagen, arachidonic acid, and ristocetin. In group I, samples were also obtained after HD. Platelet counts did not differ among the groups. Aggregation studies showed a lower response to ADP and ristocetin in the HD patients, but not in the CAPD or in the chronic renal failure patients. The percentage of platelets with high RNA content in group I was significantly lower than in controls (3.72 +/- 1.72% vs. 9.05 +/- 3.53%, P < 0.01), but was also lower than in the remaining groups (I vs. II P < 0.01, and I vs. III P < 0.01). No differences were seen in platelet RNA content among groups II (8.67 +/- 2.73%), III (9.14 +/- 3.04%) and IV. In group I, the percentage of reticulated platelets decreased further after HD (2.14 +/- 1.09%, P < 0.01). Aggregation studies showed a significantly lower response to ADP and ristocetin in group I (P < 0.05), but not in groups II or III in comparison with controls. Aggregation response to ADP and ristocetin decreased after HD (P < 0.05). In conclusion, HD may decrease the percentage of RNA-rich platelets through elimination of the younger and more active platelets and worsen the thrombopathy present in uremic patients.

Adult

Effect of antihypertensive treatment on the increased beta 2-adrenoceptor density in patients with essential hypertension.

The effect of different antihypertensive drugs on the increased surface beta 2-adrenoceptor density in essential hypertension was evaluated to elucidate whether the possible effect of the treatment on these receptors was secondary to blood pressure decreases or a specific effect of the drugs. Thirty-nine untreated essential hypertensive patients and 28 normotensive control subjects were studied in basal conditions. Hypertensive patients were randomly assigned to three treatment groups: bisoprolol (10 mg/day, n = 15), enalapril (20 mg/day, n = 12), and verapamil SR (240 mg/day, n = 12), and were studied before and after 1 month of treatment. Plasma catecholamines were determined by a radioenzymatic assay. Surface beta 2-adrenoceptors were measured in intact lymphocytes by radioligand binding assay using the hydrophilic ligand [3H]-CGP12177. beta 2-adrenoceptor density was increased in hypertensive patients (P < .01). After treatment, mean blood pressure decreased similarly in the three groups, while plasma catecholamines showed no significant changes in any group. beta 2-adrenoceptor number decreased only in bisoprolol-treated patients (P < .05). Mean blood pressure decreases correlated with beta 2-adrenoceptor decrements only in bisoprolol-treated patients (r = 0.65, P < .05). beta 2-adrenoceptor density correlated with plasma epinephrine levels in the control group (r = -0.50, P < .01), but not in hypertensive patients before treatment. This correlation was also observed in hypertensive patients treated with bisoprolol (r = -0.52, P < .05), but not in those treated with verapamil or enalapril. Our results suggest that bisoprolol treatment reduces the increased surface beta 2-adrenoceptor density and restores its regulation by epinephrine in essential hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Reversible decrease of surface beta 2-adrenoceptor number and response in lymphocytes of patients with pheochromocytoma.

To study the effect of chronic exposure to elevated plasma catecholamines on surface beta 2-adrenoceptor density, we measured these receptors in the lymphocytes of 9 patients with pheochromocytoma as well as in 27 healthy control subjects. Binding experiments were performed on intact lymphocytes using the hydrophilic ligand [3H]-CGP12177. Lymphocyte beta 2-adrenergic response was also measured in three patients. beta 2-adrenoceptor density (p < 0.01), and isoproterenol-stimulated increase in cAMP were reduced in patients with pheochromocytoma. Both parameters normalized (p < 0.05) when patients were reevaluated 4 weeks after tumor removal, coinciding with normalization of plasma epinephrine (r = -0.95, p < 0.01) and to log of plasma norepinephrine (r = -0.58, p < 0.05) in patients. We conclude that chronic catecholamine excess induces a decrease of lymphocyte beta 2-adrenoceptor surface number and response that is reversible upon normalization of plasma catecholamine levels. This regulation is mainly dependent on plasma levels of the hormone epinephrine, but norepinephrine may also play a regulatory role at supraphysiological levels.

Adrenal Gland Neoplasms

[Intravenous calcitriol in the treatment of the refractory secondary hyperparathyroidism of terminal chronic kidney failure].

BACKGROUND: In advanced cases of secondary hyperparathyroidism (HPT) in terminal chronic renal failure, the oral treatment of calcitriol is not possible due to the development of hypercalcemia. It has been demonstrated that calcitriol directly inhibits the secretion of parathormone (PTH), independently of calcium. Therefore the intravenous administration of high and intermittent doses of calcitriol (ivVD) has been proposed as an alternative treatment for resistant HPT. METHODS: The response of PTHi to treatment over 6 months with ivVD was evaluated in 18 patients with moderate-severe HPT resistant to the classical schedules. RESULTS: An important decrease was observed in the PTHi values (basal: 698 +/- 277 pg/ml, end of treatment: 272 +/- 200; p < 0.05). Alkaline phosphatase values followed a parallel course (basal: 476 +/- 286 U/l, end of treatment: 301 +/- 276 U/l, p < 0.05). Fifty-five percent of the patients presented hypercalcemia at some time (Ca > or = 11.5 mg/dl) being controlled by a decrease in the doses of calcitriol or calcium in dialysis fluid. No response was observed in 3 patients (17%) with treatment being discontinued due to presentation of uncontrollable hypercalcemia. CONCLUSIONS: The administration of intravenous calcitriol at high and intermittent doses is effective in a considerable number of patients with hyperparathyroidism resistant to the classical oral schedules. Its use may avoid surgical parathyroidectomy in some cases.

Adult

Platelet activation during hemodialysis measured through exposure of p-selectin: analysis by flow cytometric and ultrastructural techniques.

P-selectin is a platelet protein in alpha-granules that is expressed on their membranes after platelet activation. Using a specific monoclonal antibody (RUU-2.17), we have studied platelet activation during hemodialysis with a cuprophan membrane in eight patients with uremia. Blood samples were obtained before hemodialysis from venipuncture (sample I), at the beginning of the hemodialysis from the arterial (sample II) and venous lines (sample III), and after 2 hours of hemodialysis from the venous line (sample IV). Exposure of P-selectin on platelet surface was studied by flow cytometry, and morphologic and immunocytochemical studies were performed. No differences in P-selectin expression were observed by single-labeling flow cytometry in samples I, II, and IV. However, a significant increase in fluorescence occurred in sample III (percentage of positive platelets [%PP], 18.0% +/- 6.1%) with respect to sample I (%PP, 6.9% +/- 2.0%; p < 0.01). An apparently decreased fluorescence was seen in sample IV (%PP, 8.8% +/- 3.9%) with respect to sample III. Double-labeling flow cytometry showed statistically significant differences between sample I (%PP, 7.1% +/- 2.6%) and sample III (%PP, 19.4% +/- 9.4%; p < 0.01) and IV (%PP, 19.0% +/- 10.1%; p < 0.01), but not between samples III and IV. The ultrastructural study revealed an increasing number of platelet morphologic signs of activation throughout the period of hemodialysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Intracellular calcium mobilization and activation of the Na+/H+ exchanger in platelets.

The aim of the present study was to evaluate the regulatory relationship between the cytosolic free calcium concentration ([Ca2+]i and cytosolic pH (pHi). [Ca2+]i and pHi were measured using the fluorescent dyes fura-2 and BCECF [2',7'-bis-(carboxyethyl)-5,6-carboxyfluorescein] respectively. In a medium with 1 mmol/l extracellular calcium, thrombin (2.5 units/ml) induced an increment in [Ca2+]i of 638 +/- 31 nmol/l (n = 5) and an intracellular alkalinization of 0.14 +/- 0.01 pH units (n = 8). Both responses were dependent on the concentration of thrombin, displaying a sigmoidal dose-response pattern. The intracellular alkalinization was dependent upon extracellular Na+ and was amiloride-sensitive, indicating that it was mediated by activation of the Na+/H+ exchanger. When extracellular calcium was chelated with EGTA prior to the addition of thrombin, the intracellular alkalinization was not affected (0.15 +/- 0.02 at 2.5 units/ml thrombin, n = 8). Under these circumstances, the [Ca2+]i increment represents mobilization from internal stores, reaching 157 +/- 42 nmol/l at 2.5 units/ml thrombin. When platelets were preloaded with the intracellular calcium chelator MAPTAM (1,2-bis-5-methylaminophenoxylethane-NNN'-tetraacetoxymethyl acetate) to block the increase in [Ca2+]i induced by thrombin, no increment in pHi was observed. Moreover, MAPTAM-loaded calcium-depleted platelets had a basal pHi that was more acidic than in the presence of 1 mmol/l extracellular calcium (6.93 +/- 0.09 versus 7.14 +/- 0.01, n = 26, P < 0.001). Ionomycin induced an elevation of [Ca2+]i that was accompanied by a concomitant increase in pHi, which was Na(+)-dependent and amiloride-sensitive. [Ca2+]i and pHi increases induced by ionomycin were both dependent on the concentration of ionomycin. In conclusion, an increase in [Ca2+]i is necessary for the agonist-induced activation of the Na+/H+ exchanger in platelets. Non-agonist-induced increases in [Ca2+]i seems to prompt activation of the exchanger. In addition, Ca(2+)-depleted platelets have a more acidic basal pHi, indicating that the basal level of [Ca2+]i is also important for maintaining the basal pHi.

Blood Platelets

Minimal-change glomerulopathy and carcinoma. Report of two cases and review of the literature.

We describe 2 patients with minimal-change glomerulopathy (MCG) associated with an undifferentiated carcinoma of unknown origin and urothelial carcinoma. Oliguric acute renal failure and histopathological changes consistent with acute tubular necrosis were also observed. Fourteen other cases of MCG complicating solid tumors reported in the literature are reviewed. MCG should be included in the nephropathies which cause nephrotic syndrome in adult patients with carcinoma.

Acute Kidney Injury

Platelet activation on hemodialysis: influence of dialysis membranes.

During hemodialysis, platelets are activated and release alpha-granule-specific proteins. GMP-140 is a glycoprotein stored in the alpha-granules of platelets, which is selectively expressed on the plasma membrane of activated platelets. Using a specific monoclonal antibody against this protein (CD 62), we have evaluated the influence of different dialysis membranes on hemodialysis-induced platelet activation in vivo by flow cytometry in nine patients with end-stage renal disease on maintenance hemodialysis. Five membranes were evaluated: Cuprophane, cellulose acetate, polymethylmethacrylate, polysulphone and polyacrylonitrile (AN-69). Blood samples were obtained before hemodialysis and from the inlet and outlet lines five minutes after the beginning of hemodialysis. A significant increase in the GMP-140 expression was observed in samples obtained from the outlet line compared with samples obtained from the inlet line for all membranes evaluated, but the extent of this increase depended on the type of membrane used: Cuprophane 13.95 +/- 3.94%, cellulose acetate 7.4 +/- 4.52%, polymethylmethacrylate 6.93 +/- 4.6%, polysulphone 3.83 +/- 2%, and AN-69 2.14 +/- 2.19% (mean +/- SD). Cuprophane induced the highest degree of platelet activation (P < 0.05). Cellulose acetate and polymethylmethacrylate induced more platelet activation than polysulphone or AN-69 (P < 0.05). These data demonstrate that all hemodialysis membranes induce platelet activation but to a variable extent, cuprophane being the most activating membrane, cellulose acetate and polymethylmethacrylate showing an intermediate potential of activation, while the more biocompatible membranes, polysulphone and AN-69, inducing the lowest degree of platelet activation.

Adult

Abnormal cytoskeletal assembly in platelets from uremic patients.

The mechanisms involved in the hemostatic abnormality of uremic patients remain obscure. We have explored the response of normal and uremic platelets to surface activation at the ultrastructural level and analyzed changes in the composition of proteins associated with normal and uremic platelet cytoskeletons after stimulation with thrombin (0.01 and 0.1 U/ml). Cytoskeletons were obtained by extraction with Triton X-100, processed by sodium dodecylsulfate-polyacrylamide gel electrophoresis, and the presence of cytoskeletal proteins analyzed by densitometry. Under static conditions, uremic platelets spread with difficulty on formvar-coated grids. The percentage of platelets that spread fully on this polymer surface was statistically reduced compared with that of control platelets (11 +/- 1.4 vs. 21 +/- 1.6; P < 0.05). An impairment of cytoskeletal organization was observed in resting uremic platelets but abnormalities were more evident after thrombin activation. The incorporation of actin into the cytoskeletons of thrombin-stimulated uremic platelets was significantly reduced with respect to controls (6 +/- 3% vs. 29 +/- 5%; P < 0.01 after 0.01 U/ml and 28 +/- 9% vs. 59 +/- 10%; P < 0.05 after 0.1 U/ml). Decreased associations of actin-binding protein (P < 0.01), alpha-actinin (P < 0.05), and tropomyosin (P < 0.05) with the cytoskeletons of uremic platelets were also noted. No difference was observed for the incorporation of myosin into the cytoskeletons of activated uremic platelets. These results suggest functional and biochemical alterations of the platelet cytoskeleton in uremia, which may contribute to the impairment of platelet function observed in uremic patients.

Adult

Calciphylaxis in a hemodialysis patient: appearance after parathyroidectomy during a psoriatic flare.

Chronic renal failure patients are prone to soft tissue calcifications. A phenomenon of acute ischemic skin necrosis and dermohypodermic arteriolar medial calcification has been described recently in patients with chronic renal failure and secondary hyperparathyroidism (HPT). This phenomenon, termed calciphylaxis, occurs in response to certain factors, the most important of which appears to be an elevated blood calcium-phosphate product. Accordingly, parathyroidectomy in addition to normalization of calcium-phosphate product has been proposed as the only effective therapeutic approach for this condition. We describe a case of chronic renal failure with severe secondary HPT in which the patient developed calciphylaxis 4 days after the appearance of a psoriatic flare. Four months before, a subtotal parathyroidectomy was performed for severe HPT and at the time the ulcerations appeared, blood calcium-phosphate product was correct. Etiological and physiopathological aspects of calciphylaxis are discussed.

Calciphylaxis

Recombinant human erythropoietin treatment improves platelet function in uremic patients.

The effect of recombinant human erythropoietin (rHuEPO) on primary hemostasis was tested in 19 hemodialyzed patients. Bleeding time, platelet aggregation and platelet interaction with vessel subendothelium (SE) under flow conditions were determined before treatment and after patients reached hematocrits greater than or equal to 30%. Two thrombotic events (an acute myocardial infarction and an AV fistula clotting) were recorded during the early stages of treatment. A shortening of average bleeding times (P less than 0.01), an increase in platelet count (P less than 0.01) and an improvement of platelet aggregation (P less than 0.01) and of platelet-SE interaction (P less than 0.01) were observed. A low correlation index was found between hematocrit and bleeding time (r = -0.351, P less than 0.05). To assess a possible effect of rHuEPO on platelet function, the same parameters were evaluated before and after receiving three doses of rHuEPO (40 U/kg i.v. post-hemodialysis) in 14 of the patients. No changes in platelet or erythrocyte counts were observed, the mean bleeding time remained unchanged, but platelet aggregation induced by arachidonic acid (P less than 0.05), ADP (P less than 0.01) and ristocetin (P less than 0.05) improved. Perfusion studies confirmed moderate but significant increases in the parameters that quantify platelet-SE interaction (P less than 0.05). Improvement of ADP-induced aggregation correlated with the increase of platelet adhesion to SE (r = 0.675, P less than 0.05). We conclude that rHuEPO treatment improves primary hemostasis in uremia through an increase of red cell mass but also through a beneficial effect on platelet function, which is independent of the hematocrit rise.

Adult

Arginine vasopressin infusion increases plasma levels of atrial natriuretic factor in humans.

Seven normal subjects underwent sequential 20-min infusion of arginine vasopressin (AVP) at 0.5 and 2 ng/(kg.min) and a complete right-side heart hemodynamic evaluation during the study to analyze the effect of this hormone on atrial natriuretic factor (ANF) secretion in humans and to elucidate whether this effect was primary or secondary to the hemodynamic or hormonal changes induced by AVP. Plasma ANF levels increased at the end of the first (P less than 0.05) and second (P less than 0.01) infusion periods. No significant changes in mean arterial, pulmonary artery, right and left atrial pressures were recorded during the study. Cardiac output (P less than 0.05) and heart rate (P less than 0.05) decreased, while total vascular resistances (P less than 0.05) increased with respect to basal values in both infusion periods. Plasma renin activity decreased (P less than 0.01) at the end of the infusion, while plasma aldosterone, epinephrine and norepinephrine showed no significant changes. We conclude that arginine vasopressin increases plasma ANF levels in humans and that this effect cannot be ascribed to hemodynamic or hormonal changes induced by this hormone, suggesting a direct effect of vasopressin on the atrial myocyte.

Adult

Tumor markers in chronic renal failure and hemodialysis patients.

Serum levels and the incidence of elevated levels of several tumor markers were measured in 30 patients with chronic renal failure (CRF) of different degrees, as well as in 36 hemodialyzed (HD) patients without clinical evidence of neoplasia. The tumor markers evaluated were carcinoembryonic antigen (CEA), CA 125, CA 15.3, CA 19.9, CA 50, alpha-fetoprotein, neuron-specific enolase (NSE), squamous cell carcinoma antigen (SCC), prostatic acid phosphatase and prostatic-specific antigen. Serum levels of CEA were above the cutoff limit in 33% of patients with CRF and 47% of HD patients, CA 50 was higher than normal values in 37 and 44% of patients, respectively. SCC was elevated in 43 and 72% of patients, respectively. Serum levels of CA 125 were elevated in 18% of patients with CRF and NSE in 36% of HD patients. In CRF several tumor markers (CEA, SCC, CA 50 and NSE) show a high false positive rate and may be unreliable for monitoring malignancies in uremic patients, while the other markers evaluated appear to maintain their specificity in this situation.

Adult

[Late recurrence in pheochromocytoma: need for a long term follow up].

Pheochromocytoma is a catecholamine secreting tumor which has been traditionally considered as a potentially curable cause of hypertension. However, the existence of malignant pheochromocytomas as well as the problem which the recurrence of benign pheochromocytomas present, make the eradication of this tumor more complicated. It is note worthy the difficulty in localizing recurrent pheochromocytomas as well as the prognostic interest that presents the possibility of differentiating between recurrence and metastasis. We refer the case of a female patient suffering benign adrenal pheochromocytoma, who, 10 years it was surgically removed, presented a relapse of symptoms, and was diagnosed of extra-adrenal pheochromocytoma, in Zuckerkandl organ. The importance of performing a long term post-surgical follow-up in these patients is stressed.

Adrenal Gland Neoplasms